Juntti-Berggren L, Larsson O, Rorsman P, Ammälä C, Bokvist K, Wåhlander K, Nicotera P, Dypbukt J, Orrenius S, Hallberg A
Rolf Luft Center for Diabetes Research, Department of Endocrinology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Science. 1993 Jul 2;261(5117):86-90. doi: 10.1126/science.7686306.
Type I diabetes [insulin-dependent diabetes mellitus (IDDM)] is an autoimmune disease associated with the destruction of pancreatic beta cells. Serum from patients with IDDM increased L-type calcium channel activity of insulin-producing cells and of GH3 cells derived from a pituitary tumor. The subsequent increase in the concentration of free cytoplasmic Ca2+ ([Ca2+]i) was associated with DNA fragmentation typical of programmed cell death or apoptosis. These effects of the serum were prevented by adding a blocker of voltage-activated L-type Ca2+ channels. When the serum was depleted of immunoglobulin M (IgM), it no longer affected [Ca2+]i. An IgM-mediated increase in Ca2+ influx may thus be part of the autoimmune reaction associated with IDDM and contribute to the destruction of beta cells in vivo.
1型糖尿病[胰岛素依赖型糖尿病（IDDM）]是一种与胰腺β细胞破坏相关的自身免疫性疾病。IDDM患者的血清增加了胰岛素产生细胞和源自垂体肿瘤的GH3细胞的L型钙通道活性。随后游离细胞质Ca2+浓度（[Ca2+]i）的增加与程序性细胞死亡或凋亡典型的DNA片段化有关。通过添加电压激活的L型Ca2+通道阻滞剂可防止血清的这些作用。当血清中的免疫球蛋白M（IgM）被耗尽时，它不再影响[Ca2+]i。因此，IgM介导的Ca2+内流增加可能是与IDDM相关的自身免疫反应的一部分，并有助于体内β细胞的破坏。
